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Smell and taste disorders

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 OPEN ACCESS Review Article

Smell and taste disorders

Abstract
Smell and taste disorders can markedly affect the quality of life. In recent Thomas Hummel1
years we have become much better in the assessment of the ability to
Basile N. Landis2
smell and taste. In addition, information is now available to say some-
thing about the prognosis of individual patients. With regard to therapy Karl-Bernd Hüttenbrink3
there also seems to be low but steady progress. Of special importance
for the treatment is the ability of the olfactory epithelium to regenerate. 1 University ENT Clinics,
Keywords: olfaction, gustation, flavor, anosmia, dysgeusia Dresden, Germany
2 University ENT Clinics, Bern,
Switzerland
3 University ENT Clinics,
Cologne, Germany

1. Introduction tem. (1) The gustatory system (N. glossopharyngeus,

In a recent review [1] three functions were assigned to
the senses of smell and taste, namely a warning of
danger, interpersonal communication and importance
for eating and drinking. These functions reflect the com-
plaints of patients with smell and taste disorders: Patient
complaints include loss of “fine taste”, inability to detect
the odour of a partner or child, and the occurrence of, for
example, food poisoning [2], [3], [4], [5].
In general the value of these senses is only recognised
when they are lost. It is assumed that about 5% of people
exhibit functional anosmia [6], [7], [8], [9]. This is largely
caused by age – above an age of 50 years 25% of people
have an impaired sense of smell [6], [10]. Interestingly,
the ability to smell appears to be a measure of the overall
health of a person: For example, smell becomes worse
the more medicines are taken [8], [11] and one’s life ex-
pectancy seems to be negatively associated with lowered
olfactory abilities [12]. Despite these relationships, relat-
ively little is known about the causes and possible treat-
ments of smell and taste disorders when this is compared
to understanding of sight and hearing disorders.
Research in the field of the chemical senses harbours
more technical difficulties with controlling olfactory,
gustatory or trigeminal stimuli than this is the case for
visual and acoustic stimuli. Due to a number of factors,
it is much easier to produce clicks of exactly 10 ms dura-
tion of a defined pitch than, for example, to generate a
peach odour of precise duration, concentration and dis-
persal rate [13]. Other special aspects arise from the
multisensory integration of information, which is very
important for smell, taste and trigeminal perception – for
example when eating a cherry. The perception of taste
results from the interplay of at least three sensory chan-
nels, namely 1. taste, 2. smell and 3. the trigeminal sys-
N. facialis, N. vagus) recognizes the basic tastes: sweet,
sour, salty, bitter and umami (glutamate). (2) The olfactory
nerve recognizes a wide range of odorants such as vanilla
or H2S (the smell of rotten eggs). When eating, the
N. olfactorius identifies all the fine nuances which trans-
form the intake of food into a culinary experience. Here,
the odour molecules are passed to the olfactory epitheli-
um via the retronasal pathway. A connoisseur of taste
therefore also has a fine sense of smell. (3) Finally, the
N. trigeminus identifies sensations such as the sharpness
of horseradish, and the cooling, tingling effect of menthol.
As almost all odours can cause a trigeminal sensation,
the trigeminal nerve plays a key role in the perception of
odours.
Other chemo-sensitive systems that have been described
for animals, such as the vomeronasal organ [14], [15]
and the N. terminalis [16], probably have no importance
in adult people.
2. The sense of smell
2.1 Physiology and anatomy
The olfactory epithelium is located on the roof of the
nasal cavity and hence does not lie in the main airflow
stream of breathing [17]. This narrow location called ol-
factory cleft is open for the ortho- but also retronasal
airflow. This means odours can reach the olfactory cleft
via sniffing through the nostrils but also via the
nasopharynx by passing retronasally into the nose when
eating or drinking. Due to this special location of the ol-
factory neuroepithelium, the local odour concentration
is partly subject to respiratory control [18]. Also, the
complex intranasal anatomical conditions [19] explain
why smell disorders can occur after nose operations with

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 Hummel et al.: Smell and taste disorders
anatomical changes far from the olfactory regions [20].
There are also particular clinical pictures with patients
able to recognize retronasal stimuli but not orthonasal
odors – and vice-versa [21], [22].
The olfactory receptor neurons (ORNs) are located in the
olfactory epithelium and thus directly exposed to environ-
mental conditions (temperature, toxins, trauma, etc.).
This could be a reason why olfactory cells regenerate
continuously [23], [24]. This ability to regenerate probably
diminishes with increasing age [25], [26], which could
be the cause of the increasing susceptibility of the olfact-
ory system to viral diseases and decreased olfactory
function with age [27], [28].
Before odours can cause excitation of the olfactory recept-
ors, which are located on cilia on the bipolar olfactory
receptor neurons (ORNs), the odour molecules must first
diffuse through the mucous on the mucous membrane
[29]. The proteins which are dissolved in the mucous, but
which have been little studied [30], [31], probably act as
transport proteins for lipophilic odours, through the mu-
cous to the receptor. Little is also known about how
odours are metabolized within the human olfactory mu-
cous membrane and it is not yet clear if the mucous
membrane has local growth factors interacting with the
ORN homeostasis [32].
About 1,000 olfactory receptors are coded in the human
genome [33], although only about 380 of these receptors
are functionally expressed within the human olfactory
epithelium [34]. Each ORN expresses a specific receptor
type. These receptors are not highly specific to a single
odorant, rather single odorants evidently bind to different
receptor types. As ORNs that express the same receptor
type send their axons to the same glomeruli in the olfact-
ory bulb, the activation of different receptor types causes
different excitation patterns in the bulb. These different
excitation patterns are the basis for the quality coding of
odours. The participation of the hippocampus and the
amygdala in the processing of odour information partly
explains the emotional character of odours and the key
role of odours in the recalling of (typically children’s)
memory records [35]. The physiology of the cerebral
processing of odour impressions is not wholly clear [36],
[37]. However, the orbitofrontal cortex plays a major role
in the conscious perception of odours [36]; other import-
ant structures are the piriform cortex, the amygdala, the
hippocampus, the thalamus, the nucleus accumbens,
and the cerebellum.
Olfactory sensitivity depends on age and gender. Women
are superior to men in virtually all aspects of olfactory
function [38]. The exact reason for this is unclear; hor-
monal effect have been discussed but remain a matter
of debate; possibly the higher social awareness of women
also plays a role, in so far that women, more than men,
show interest in odours as social signals (e.g. body
odours, food odours). Accordingly, women on average
suffer more than men from loss of smell [5].
The reduced ability to smell with increasing age is long
known [10], [39] and is also partly due to the decrease
in ORNs [26]. This presbyosmia is, however, not unavoid-
GMS Current Topics in Otorhinolaryngology - Head and Neck Surgery 2011, Vol. 10, ISSN 1865-1011
able, but is also an expression of overall health [11];
people who have “aged well” and do not take any medic-
ation seem to have essentially normal smell thresholds
[40]. The slow, age-related loss of smell is however not
always noticed or complained about; the loss of “fine
taste” is apparently partly offset by gustatory and trigem-
inal sensations [41], [42].
2.2 Definition of olfactory disorders
Quantitative smelling disorders
Anosmia describes the lack of ability to smell, and specific
anosmia describes the inability to smell a specific odour,
whereas the vast majority of odors are normally perceived.
Such specific anosmias have been described for a series
of different odours [43] and are considered a physiologic-
al phenomenon. The occurrence of these specific anos-
mias indicates that specific receptors are necessary for
perceiving a specific odour [44]. Specific anosmias have
little clinical importance. The term functional anosmia
refers to a significantly reduced ability to smell, although
some smell sensations can be present. These do however
not give patients a normal ability to smell which would
be meaningful in daily life. Hyposmia refers to a reduced
ability to smell, and hyperosmia to an enhanced ability
to smell. Hyposmic conditions are common, but hyperos-
mias are very rare; they have been encountered, for ex-
ample, after exposure to toxic vapours [45] and with mi-
granes [46].
Qualitative smell disorders
A distinction is made here between parosmia and
phantosmia. The latter describes the perception of odours
in the absence of a relevant odour source, and the former
describes the qualitative “wrong” perception of odours.
Patients, for example, perceive something after being
presented with an odour of roses, which it is not the ex-
pected odour of roses, but rather a distorted and often
undefined odorous perception. Exactly the same odour
is also perceived by parosmia patients after being
presented other odours, meaning that many odours
qualitatively smell more or less the same. In general these
“other” odour sensations are experienced as unpleasant.
And they are generally only described in vague terms, for
example as “chemical”. Parosmia is typically associated
with reduced olfactory sensitivity. It can occur after viral
infections of the upper respiratory tract or after skull-brain
traumas. In rare cases parosmia can be caused by sinus-
itis by odours which arise in the infected paranasal si-
nuses. Many patients having qualitative smell disorders
are also found to simultaneously have symptoms of de-
pression (overview in [47]).
A simple classification of qualitative smell disorders can
be made based on 3 criteria: daily/not daily (1 or 0 points
resp.); intense/not intense (1 or 0 points resp.); social or
other notable consequences (e.g. weight in-
crease/loss)/no social or other consequences (1 or 0
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 Hummel et al.: Smell and taste disorders
points resp.): The sum of the points gives the degree of
parosmia or phantosmia (0 to 3rd degree) [48]. The
graduation of parosmia was recently investigated for its
clinical usefulness by means of a questionnaire. This first
study appears very promising and a further improved
questionnaire about clinical parosmia and phantosmia
is in preparation [49].
Many patients with smell disorders who visit special
clinics also complain of a loss of taste [50]. Only about
10% of the patients complain of an isolated loss of taste;
there is however only a measurable loss of taste in less
than 5% of these patients [50]. On the other hand, a loss
of smell is generally accompanied by a slight reduction
in the ability to taste, probably due to the lack of central
nervous system interactions between the chemical senses
[51], [52]; see also [53].
2.3 Aetiology of olfactory disorders
The four main causes of smell disorders are (1) trauma,
(2) viral infections, (3) nasal causes such as sinusitis or
polyposis nasi and (4) smell disorders associated with
aging or neurological illnesses such as Parkinson’s dis-
ease or Alzheimer’s disease. Smell disorders after a
trauma are possible due to severance of the fila olfactoria
[54], and probably also the contusion of secondary olfact-
ory-related areas of the brain such as the orbitofrontal
cortex [55]. Viral infections are assumed to cause damage
to the ORNs [56]. However, the triggering agent is still
unclear [57], [58].
With nasal causes one assumes an inflammation-related
functional impairment or shift of the mechanical access
to the olfactory epithelium [59], [60]. One of the first
symptoms of both Alzheimer’s disease [61] and also
Parkinson’s disease [62], [63] is a decrease in olfactory
sensitivity. Interestingly, this precedes the motoric
symptoms of Parkinson’s disease by 4–6 years (Table 1,
Table 2).
Smell disorders accompanying neurological illnesses
Smell disorders accompany many neurodegenerative ill-
nesses [64], [65] and are important for their early and
differential diagnosis. They are present in over 95% of
patients with idiopathic Parkinson’s syndrome (IPS) [66]
– if one uses the smell function of young, healthy persons
as the standard value. When using age-related standard
values [67] almost 75% of IPS patients can still be dia-
gnosed with an olfactory dysfunction (Table 2). Here, the
majority of the patients have severe hyposmia, or already
anosmia. For this reason, the diagnosis of IPS should be
reconsidered in patients with a normal ability to smell
suspected to suffer from IPS. The loss of smell occurs
very early during the progression of IPS, meaning that it
can be considered to be the first symptom of the illness.
It is suspected that the olfactory disorders precede the
motoric symptoms by ca. 4–6 years [62], [66], [68], [69].
The primary cause of the smell disorder accompanying
IPS is unknown; with solely non-specific changes in peri-
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pheral olfactory structures, it is however assumed to in-
volve central brain structures [68], [70].
Smell disorders also occur with other Parkinson’s syn-
dromes such as Lewy-Body dementia and multi-system
atrophy [71], [72]. Huntington’s disease is associated
with moderate hyposmia [73]. Mild olfactory disorders
have also been described for some heredoataxias and
motor neuron diseases [74], [75].
Similarly severe olfactory disorders to those found with
IPS have been observed with Alzheimer’s disease (AD).
Meta analysis of studies carried out up until now on ol-
factory disorders accompanying AD and IPS showed no
differences in the test results of diagnostic use [74]. The
smell disorder with AD also represents an early symptom
of the disease [76]. Treatment of the olfactory dysfunction
associated with neurodegenerative illnesses has hitherto
not been possible. Due to its early occurrence with IPS
and AD this disorder does however have importance for
diagnosing these diseases, namely patients with an un-
explained loss of smell have a higher risk of subsequently
developing IPS or AD. For this reason, the Guidelines of
the “Deutsche Gesellschaft für HNO-Heilkunde” (http://
www.awmf.org/leitlinien/detail/ll/017-050.html) state
that a neurological examination is recommended for pa-
tients with unexplained smell disorders on completion of
the ENT diagnostics in the event of there being irregular-
ities in the anamnesis and examination.
There are many other causes of smell disorders, including
congenital anosmia, exposure to toxic substances, psy-
chiatric illnesses such as schizophrenia and depression,
epilepsy or systemic diseases such as sarcoidosis, lupus
erythematodes, as well as endocrine disorders like hypo-
thyroidism, diabetes or isolated organ deficiencies like
kidney failure and liver failure or tumors (e.g. esthesioneur-
oblastoma and other intranasal carcinomas and benign
or malignant brain tumours). Latrogenic causes of smell
disorders have been cited as neurosurgical operations,
radiotherapy, intake of medicines (Table 3) and occasion-
ally ENT procedures. Often the cause of the smell disorder
cannot be found with certainty; some of the idiopathic
dysosmias are due to inflammation [77] or the early onset
of Parkinson’s disease [66].
2.4 Patient examination
The first step is a detailed patient’s history (see http://
wwwold.tu-dresden.de/medkhno/riechen_schmecken/
download.htm). This should cover eating, drinking and
smoking habits, accidents, operations and medicines
taken as well as URTIs preceding the olfactory disorders
and the presence of nasal complaints (nasal obstruction,
rhinorrhea, facial pain). Questions must also be asked
about thyroid function, depression, lupus erythematodes,
zinc deficiency, vitamin A or B12 deficiency and allergies.
The focus of the physical examination is the ENT examin-
ation. The endoscopic examination of the nose must in
particular check for polyps or other swellings in the area
of the middle turbinate or olfactory cleft region, which
can block access of odor molecules to the olfactory epi-
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 Hummel et al.: Smell and taste disorders

Table 1:Features of post-trauma, post-viral/infection and sinunasal smell disorders

Table 2: Relative degree of olfactory dysfunction associated with neurodegenerative diseases.

+++: high degree of smell loss; 0/(+): no smell loss or slight smell loss.
The majority of the findings are based on studies on small groups of patients.

Table 3: Medicines which may cause smell disorders

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 Hummel et al.: Smell and taste disorders
thelium meaning the smell function disappears but the
ability to breathe is unimpaired. Such a condition has
been described and named “olfactory cleft disease” [78],
consisting of an isolated obstruction of the olfactory cleft.
This is the reason why rhinomanometry is not entirely
useful for evaluating smell function (see also [79]).
A neurological consultation is often recommended. MRI
examinations may be necessary, for example for
idiopathic smell disorders and for cerebral causes of smell
disorders such as brain tumours, blood vessel malforma-
tion or changes, bleeding or infarctions. Furthermore,
MRI is still the gold standard for evaluating congenital
smell disorders due to aplasia or hypoplasia of an olfact-
ory bulb.
2.5 Testing the ability to smell
Psychophysical testing of orthonasal olfaction
A distinction must be made between screening tests for
orthonasal olfaction and other examination procedures.
Tests for screening olfaction must be able to distinguish
between “healthy” and “ill”. A series of procedures are
available for this [80], almost all of which involve identi-
fying odours. The “Sniffin‘ Sticks” test in its various ver-
sions is introduced below. This test is recommended by
the Working Group on Olfaction and Gustation of the
German Society for ENT Medicine.
The screening test with the reusable “Sniffin’ Sticks” [81],
[82] involves smelling 12 odours and gives a comprehens-
ive result [83]. There are also shortened tests with 3 [84]
or 5 odor probes [85] which give good clinical data but
only allow for limited conclusions to be drawn. The odors
are distributed in felt-pen like devices. On removal of the
cap the odour is released. The pen is held for ca. 3
seconds about 2 cm under both nostrils. The patients are
asked to identify the odour from a list of 4 choices. The
procedure is based on a forced choice paradigm. The
overall result is the sum of the correct answers.
In addition to the screening tests, standardised and val-
idated tests for detailed assessment of olfaction function
have been developed. They allow the assessment of
various olfactory functions such as the detection
threshold for one or more odours, the ability to discrimin-
ate between or to identify odours, or to investigate the
smell memory and the ranking of above-threshold odour
concentrations. The reason for these diverse tests is the
assumption that different tests concern different struc-
tures related to the processing of olfactory information
([86], [87], [88], but also see [89], [90]). Sniffin’ Sticks
permit detailed evaluation of the sense of smell [67]. The
test is subdivided into threshold, discrimination and
identification tests, with the later two being supra-
threshold tests. In order to increase the reliability of the
measurements, each patient must choose an answer
even if he is not sure or not perceiving any odour at all
(“forced choice paradigm”). The threshold test indicates
the concentration at which the odour is reliably detected.
The odorants most frequently used are n-butanol or
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phenylethyl alcohol [91], because of their minimal trigem-
inal components. For this test the patient wears a blind-
fold. The concentration of the solutions is based on a di-
lution series of 16 steps starting from a 4% concentration
(dilution 1:2). The patient is passed 3 sticks one after the
other. One of these sticks bears the odour, the other two
only the odourless solvent. The sequence of the sticks is
random. The test person must identify the odour-contain-
ing stick. If the patients choice was wrong, the concentra-
tion is increased stepwise. As soon as the test person
identifies the correct stick two times in a row and hence
has exceeded the odour threshold, this represents the
first turning point. Now the pen with the next lower con-
centration is used. The concentration is lowered until the
odour threshold is passed through again and the test
person can no longer pick out the correct pen. This is
then the second turning point. The concentration is then
increased again, etc. This procedure is continued until 7
such turning points have been reached. The determin-
ation of the odour threshold is calculated as the average
of the last 4 turning points. The discrimination test tests
the ability of the test person to distinguish odours. The
blindfolded test person is given 3 sticks, two of which
have the same odour and one a different odour. The test
person must determine the odd stick, but is only allowed
to smell each stick once. The whole test consists of 16
or 32 triplets [67], [92]. The identification test is similar
to the University of Pennsylvania Smell Identification Test
(UPSIT) [93]. However, the odours are present in stick
form and only 16 or 32 odours are tested [67], [92]. This
sub-test can also be done by the patients themselves
[94]. After completion of the testing, the results of the
3 individual tests are added together to give a summed
value (SDI value). Freeware for carrying out the tests and
documenting the results is available (http://wwwold.
tu-dresden.de/medkhno/riechen_schmecken/
download.htm).
Extensive smell tests allow differentiation between nor-
mosmia, hyposmia and anosmia. The commercial avail-
ability of these tests and their standardised use in various
centres mean that different clinical tests can be com-
pared. Other recently developed tests are based, for ex-
ample, on measurement of the sniffing behaviour (e.g.
CompuSniff Test: [95]). The clinical value of these tests
still has to be evaluated.
Psychophysical testing of retronasal olfaction
The first clinical assessment of patients that included
retronasal test results was carried out by Güttich [96],
[97]. The initial goal was to detect malingerers. However,
the proposed test was too unstructured and bears little
clinical value for the detection of malingerers [98]. There
is today a standardised psychophysical test available for
studying retronasal olfaction [99], [100]. This involves
placing a so-called “Schmeckpulver” (taste powder) in
the mouth (20 different powder-form foods and spices,
for example cinnamon) and asking the patient to identify
the taste from a list of 4 choices. This relatively simple
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 Hummel et al.: Smell and taste disorders
test can be prepared by oneself [101]. A very similar test
was proposed recently [85]. This test allows for an evalu-
ation of the clinically encountered claim of some patients
that he/she has no smell, but that flavour would not be
impaired [21].
Electrophysiological procedures to study
olfaction
Objective testing of smell disorders can be performed
using olfactory event-related potentials (OERPs) [102].
The olfactometer here must allow presentation of chem-
ical stimuli of defined duration, concentration and stimu-
lus rise time (for details see [103], [104]). If there is an
OEP, one can assume that there is an ability to smell. As
such, this signal is primarily of importance for medico-
legal questions. Psychophysical assessed anosmia does
not exclude a residual ability to smell [105], [106]. The
latest methods allow the monitoring of the propagation
of olfactory activation in the brain on the millisecond
scale, meaning that a novel appraisal of smell disorders
could be possible [107].
Besides determining OERPs, it is also possible to determ-
ine peripheral mucous membrane potentials in humans
(so-called electro-olfactograms) directly from the olfactory
regions [108]. Although this technique allows to investig-
ate, for example, differences in the processing of individu-
al odours [109], the current clinical value in medico-legal
cases or individual patients is limited. This is due to a
relatively high inter-individual variability of EOG responses.
Volumetric evaluation of the bulbus olfactorius
(BO)
The BO is deemed to be the relay station between the
peripheral olfactory system and central brain structures.
The high plasticity of the BO is maintained by constant
neurogenesis, which in turn appears to reflect the degree
of afferent neuronal activity. The most obvious effect of
olfactory deprivation is a large reduction of the BO
volume, for example in those with congenital smell dis-
orders [110], [111], [112], [113]. Supporting evidence
for the BO plasticity are recent findings that show, the
bulb volume to increase again with improved smell func-
tion [114], [115].
The volume of other olfactory-related brain structures
also appears to decrease as a function of olfactory loss
[116], [117], [118]. The question now, however, is how
these findings can be used for the assessment of individu-
al patients.
Functional magnetic resonance imaging (FMRI)
FMRI uses the so-called BOLD effect (Blood Oxygenation
Level Dependent Effect) to measure blood flow changes
in the brain. The background is that neuronal activity in-
creases the blood flow in this region. Not only can it be
determined when an activation takes place in the brain,
but also where this activation takes place [119], [120].
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Due to the high variability of the results and non-stand-
ardised test protocols, the results attained using this
technique have up until now not been able to be routinely
used in a clinical setting.
Biopsies from the olfactory regions
Numerous publications in recent years have described
the value of biopsies from the olfactory regions [121],
[122], [123]. Although conclusions about groups of pa-
tients have been fascinating, there are many unanswered
questions about the clinical application to individuals. In
other words, unambiguous assignment of a biopsy dia-
gnosis to a functional condition is currently not possible.
2.6 Treatment of smell disorders
There are only limited treatments available for smell dis-
orders. A proven effective treatment is only available
where nasal illnesses causes the smell disorder (for an
overview see [60]). The focus here is on surgical treat-
ment (polypectomy, pansinus procedures) and the applic-
ation of corticosteroids. With regards to surgical and also
non-surgical treatments, the so-called olfactory cleft dis-
ease is particularly difficult to treat [78], [124]; this in-
volves isolated swelling in the olfactory cleft area.
Predictive factors
The prognosis for a smell disorder basically depends on
its cause. Age-related and congenital smell disorders
cannot be treated successfully. For post-traumatic anos-
mia, full spontaneous remissions has been observed
years after the loss of smell [125]. This is, however rare.
In 10 to 20% of cases of post-traumatic anosmias there
is partial remission over the years, whereas the recovery
rate is much better for patients with post- infectious ol-
factory disorders. This figure is about 60% in cases of
post-infection smell disorders. Favourable factors for re-
mission of post-infection or post-trauma anosmia are as
high as possible residual ability to smell, female gender,
youthful age, non-smoker, initial parosmia, absence of
left and right differences in the smell function, and as
large as possible amplitudes of the chemosensory evoked
potentials to trigeminal stimuli. Also, the duration of the
smell disorder is of relevance for the prognosis.
With regards to surgically treated smell disorders, the
best results are obtained for women who are aspirin-in-
tolerant in the event of eosinophilia and polyposis. It has
to be noted that these patients have severely altered ol-
factory function before treatment and thus improve a lot
after treatment. Age and number of previous operations
have little bearing on the success of the operation on the
smell disorder. With regards to the smell function, septum
operations, for example, only result in significant improve-
ment in 13% of patients, whilst with paranasal sinus op-
erations this figure is 23% [126], [127]. The relatively low
success rate indicates on the one hand that there is room
for improvement and on the other hand that the olfactory
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 Hummel et al.: Smell and taste disorders
impairment before surgery is much more moderate than
in polyposis patients. Consequently, the olfactory changes
are less impressive and less noticed by the patients.
Non-surgical treatment of sinunasal smell
disorders
Corticoids are used as topical and systemic treatments
of sinunasal disease [128]. Systemic treatment is accom-
panied by problematic side-effects, meaning that these
drugs are generally not used for longer than 2–3 weeks.
An exception is the occasional long-term use of prednisols
at a dose of 2–5 mg/d, which is effective for some pa-
tients. Most often the use of systemic corticoids is in the
form of an intensive course of cortisone, for example
starting with a dose of 40 mg (administered at 09:00 in
the morning) and then reducing this every second day by
5 mg. This procedure also appears useful for idiopathic
smell disorders in order to rule out an inflammatory smell
disorder, which is not always macroscopically visible. A
certain percentage of these patients respond with an
improvement in their ability to smell [77], [129].
If these systemic treatments are successful, local cortic-
oids should then be administered. However, there is often
no long-term maintenance of the ability to smell [77],
[130] with topical steroids alone. A possible cause is that
topical steroids do not reach the olfactory cleft due to the
filtering function of the nose [131], [132]. It may also be
that the inflammation that responds to systemic steroids
but not to local steroids is not in the nose but at a level
higher, e.g., in the olfactory bulb.
Another approach for non-surgical treatment of sinunasal
smell disorders is the local, topical use of Na-citrulline
[133], dropped into the olfactory cleft. The results of this
first study in normal subjects have never been tried in
patients with a double-blind follow-up.
Non-surgical treatment of other smell disorders
With regard to the treatment of other, non-sinunasal smell
disorders, treatments, which are not proven to be efficient
include treatment with oestrogens ([134] but see also
[50]), zinc [135], [136], [137], minocycline [138],
vitamin A at a dose of 10,000 I.E. oral over 4 weeks
([139] – see also [140], [141]).
There are promising approaches but these are also being
controversially debated, above all because blinded stud-
ies have not been undertaken. These include the use of
acupuncture ([142] – see criticism in [143]) and the
transcranial magnetic stimulation for parosmia and
phantosmia ([144] – see criticism in [145]). Other non-
blinded studies report the effectiveness of caroverine for
smell disorders. Quint et al. [137] reported significant
improvements in smell after a 4 week course of carover-
ine, an NMDA antagonist which is also used for treating
tinnitus. In a further study Hummel et al. [146] showed
that alpha lipoic acid also had a positive effect for patients
with post-infection smell disorders. Other concepts include
utilizing the effectiveness of phosphodiesterase inhibitors
GMS Current Topics in Otorhinolaryngology - Head and Neck Surgery 2011, Vol. 10, ISSN 1865-1011
such as pentoxifylline [147] or theophylline [148]. Hirsch
et al. [149] published results of pilot experiments on the
effectiveness of a series of medicines. Although none of
these pilot studies was convincing, however the publica-
tion put forward a number of interesting proposals for
future studies. In a more recent study the effectiveness
of smell training [150] showed promising results. The
simple instruction to patients is to smell 4 different odours
each morning and each evening for a period of 4–6
months; the instruction is not to sniff as often as possible.
The so-called odour gymnastics result in improvements
in about 25% of patients. In contrast, an improvement of
only about 7% was found in patients who do not carry out
such training.
Many of these studies are promising. In general, however,
the mentioned studies are not able to separate the effect
of the treatment from possible partial spontaneous remis-
sion. Blinded studies in large groups of patients are re-
quired for this.
More can be speculated about the future. The autologous
replanting of previously removed and amplified olfactory
cells appears possible, as does the local use of growth
factors and the use of electronic sensors and their attach-
ment to the olfactory bulb. All these ideas are based on
the plasticity of the olfactory system.
3. The sense of taste
3.1 Physiology
Gustatory receptor cells are present in the taste buds,
which in turn are in the macroscopically visible tongue
papillae. Taste cells, being primary sense cells, are able
to regenerate and have a half-life of about 15 days [151],
[152]. The receptor cells on the base of the taste buds
are innervated by afferent neurons. One individual taste
bud can be innervated by several afferent neurons – a
single afferent neuron can however also innervate several
taste buds (for overview see [153]).
The transduction of acid stimuli occurs by blocking of the
K+-channels in the membrane of taste receptors. A poten-
tial-independent Na+-channel is involved in the trans-
duction process for salty stimuli. In contrast, the transduc-
tion of sweet and bitter stimuli is associated with specific
membrane receptors which are coupled to second-mes-
senger systems (cAMP and IP3) (for overview see [153]).
Interestingly, there are about 30 different bitter receptors,
which is indicative of the importance of this system [154]!
Taste sensations are transported via 3 cranial nerves:
(1) The sensory branch of the intermediate nerve (N. Fa-
cialis) that innervates taste receptors on the anterior third
of the tongue (chorda tympani) and the palate (N. pet-
rosus superficialis); (2) The N. glossopharyngeus innerv-
ates taste receptors on the back of the tongue; (3) The
N. vagus (N. laryngeus superior) innervates taste recept-
ors in the oropharynx and the pharyngeal portion of the
epiglottis. There are however also taste receptors in the
small intestine [155]. In addition, the N. trigeminus is
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 Hummel et al.: Smell and taste disorders
also involved with the transfer of sensations such as the
temperature, texture and “hotness” of food (e.g. pepper).
This redundancy is probably the reason why the loss of
the ability to taste is rarer than loss of smell and indicates
the importance of this system. For the processing of the
taste information by the central nervous system, very high
importance is attached to the brain stem, the thalamus
and the anterior insula.
Taste sensitivity diminishes with age, but less strongly
than smell sensitivity [156]. As is the case with smell,
women are more sensitive to taste than men [157].
Factors such as saliva secretion play a key role for taste
[158]. Taste is very closely connected with the retronasal
perception of odours [159].
3.2 Definition of gustatory disorders
Ageusia is a complete loss of the ability to taste, and hy-
pogeusia a partial loss of the ability to taste. Hypergeusia
refers to enhanced gustatory sensitivity. Ageusia is very
rare due to the redundant gustatory innervation of the
tongue. Of the patients who go to special clinics for their
smell or taste disorders, only about 5% of them actually
have a measurable taste impairment [50]. In a recent
survey in 761 volunteers (age range 5–89 years) there
was no case of ageusia [160]. Interestingly, a one-sided
ageusia, for example after severing the chorda tympani
or a tumour, is only rarely reported by the patient but
regularly found if taste function is measured on each side
[161], [162].
The most common taste disorder by far is dysgeusia, an
impaired taste sensation, which occurs in about 34% of
all patients going to clinics for people with smell and taste
disorders [50]. Taste stimuli are perceived differently
than normal, and often as metallic or bitter. Taste and/or
smell hallucinations have been described for epilepsies
and schizophrenias; sweet dysgeusia sometimes reflects
a first sign of lung tumours [163].
3.3 Aetiology of taste disorders
Only about 5% of all patients who visit special clinics for
smell and taste disorders actually suffer from taste dis-
orders. The vast majority have smell disorders due to
altered odour perception [50]. The main causes of taste
disorders are (1) head trauma, (2) infections of the upper
respiratory tract, (3) exposure to toxic substances, (4)
iatrogenic causes (e.g. dental treatment or exposure to
radiation), (5) medicines and (6) glossodynia, the "Burning
Mouth Syndrome" (BMS).
Head trauma can cause lesions in the regions of the
central nervous system that are important for processing
taste stimuli, for example the thalamus, brain stem and
the ventral temporal lobes. Furthermore, fractures of the
temporal bones or mandible can lead to damage to the
N. facialis, whilst the N. glossopharyngeus and N. vagus
are relatively well protected deep in the neck [164]. Even
on severing the chorda tympani there is complete recov-
ery of taste perception after several months in 20% of
GMS Current Topics in Otorhinolaryngology - Head and Neck Surgery 2011, Vol. 10, ISSN 1865-1011
cases [165]. Many medicines can cause taste disorders
(see Table 4), with most of the mechanisms involved still
being unclear (see for example [166], [167]).
BMS is regularly associated with hypogeusia, and often
there is a lasting bitter or metallic taste (for overview see
[168]). BMS is most prevalent amongst post-menopausal
women – but only very limited success has been achieved
with hormone replacement therapy [169]. In about half
of cases there was spontaneous partial remission within
6 years of the onset of the illness. Other causes of taste
disorders include tumours, bulimia, hypothyreoidismus,
Cushing‘s syndrome, diabetes mellitus and liver disease,
poor oral hygiene and the use of mouth rinses [170].
3.4 Patient examination
When examining patients with taste disorders, special
attention should be put on examining the oral cavity, the
ears and the chorda tympani. The anamnesis must ask
about the patient’s dental hygiene, saliva flow and ability
to taste. Questions about swellings, chewing behaviour,
pain in the mouth region, ear infections, oral hygiene and
associated diseases must also be asked. Examinations
using imaging techniques to rule out or prove the pres-
ence of damage to central nervous structures, and in
particular to the brain stem, thalamus and pons, may be
necessary [171]. If bacterial or mycological diseases are
suspected, swab tests should be carried out.
3.5 Testing the ability to taste
Tests are available which either assess the ability to taste
in the whole oral cavity (whole mouth test) or in specific
regions (regional test). The tests are often carried out by
presenting liquid stimuli to the front or back of the tongue
[172]. Other test methods are based on presenting the
stimuli in form of a tastant-saturated filter paper [173]
or so-called taste strips [174], [175] which is a filter paper
test with the dried tastants. The latter have the advantage
of a long shelf life; a threshold-like measurement is recor-
ded by presenting taste strips of different concentrations
– the task of the patient is to identify the flavour/taste.
Whole mouth tests correspond better to the everyday
situation for tasting. Small amounts of the flavour solution
are kept for a few seconds in the mouth. They are not
swallowed but are spat out (sip and spit method [176]).
Sugar (sweet), citric acid (acid), sodium chloride (salty)
and caffeine or quinine (bitter) are normally used as the
stimuli. Umami testing has up until now not been success-
ful. Also popular is the “three drop test” according to
Henkin [177], [172]. In this test, three drops of liquid are
presented to the patient. One of the drops is the taste
stimulus, and the other two drops are of pure water. The
threshold is defined as the concentration at which the
patient identifies the taste correctly three times in a row.
Electrogustometry is based on induction of taste percep-
tions by passing anodal current to the tongue. The sensa-
tion is similar to that if one licks the poles of a battery.
The poor correlation between electrically and chemically
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 Hummel et al.: Smell and taste disorders
Table 4: Medicines which may cause taste disorders
induced taste perception [178] limits its clinical use for
objective taste testing.
Gustatory evoked potentials can also be determined for
objective examination [179], and this is particularly useful
for medico-legal investigations. Functional MRT possibly
also has a certain role to play here [180]. The use of local
anaesthetics can be helpful for the diagnosis (and pos-
sibly also treatment) of dysgeusia: If the impaired taste
sensation disappears after removing the sensory function
of a specific area of the tongue, then an impairment of
peripheral structures must be the suspected.
3.6 Treatment of taste disorders
Special attention must be put on possible underlying ill-
nesses and on medicines taken by the patient (see
Table 4). That apart, there are no clear therapeutic
guidelines for disorders of the taste function. Treatments
with corticoids and vitamin A are often attempted, but
there is a lack of convincing clinical studies (see [135]).
The same applies for studies involving acupuncture [181].
Only for zinc gluconate (140 mg/d for 3 months) data is
available on the therapeutic effectiveness in idiopathic
dysgeusia [182], [183]. For BMS, tricyclic antidepressants
(amitryptyline, imipramine) appear to improve the abnor-
mal sensation [184]. Successful treatments have been
also carried out with clonazepam or diazepam [185];
Gabapentin appears to be ineffective [186].
4. Summary and outlook
Smell and taste disorders can markedly affect the quality
of life. In recent years validated and reliable methods
GMS Current Topics in Otorhinolaryngology - Head and Neck Surgery 2011, Vol. 10, ISSN 1865-1011
have been developed for testing the ability to smell and
taste, and these methods allow detailed investigation of
these senses. Although some of the methods are very
simple, they would, for example, allow determination of
the ability to smell and taste for quality control purposes,
both before and after surgical procedures. Even though
a few treatments currently exist, blinded studies are ab-
solutely necessary in order to separate the effect of a
treatment from the spontaneous remission of smell and
taste disorders. Of special importance for the treatment
is the ability of the olfactory epithelium to regenerate.
5. Further reading
Leitlinien der Arbeitsgemeinschaft Olfaktologie und Gus-
tologie der Deutschen HNO Gesellschaft:
http://www.tu-dresden.de/medkhno/riechen_
schmecken/LL_Riechen.pdf plus
http://www.tu-dresden.de/medkhno/riechen_
schmecken/LL_Schmecken.pdf
Doty RL. Handbook of Olfaction and Gustation: Second
Edition, Revised and Expanded (Neurological Disease
and Therapy). Informa Healthcare. 2003.
Hummel T, Welge-Lüssen, eds. Riech- und Schmeck-
störungen. Stuttgart: Georg Thieme Verlag KG; 2009.
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Corresponding author:
Prof. Dr. med. Thomas Hummel
HNO Klinik, Universitätsklinikum Dresden, Fetscherstr.
74, 01037 Dresden, Germany, Phone: 0351-458-4189,
Fax: 0351-458-4326
thummel@mail.zih.tu-dresden.de
Please cite as
Hummel T, Landis BN, Hüttenbrink KB. Smell and taste disorders. GMS
Curr Top Otorhinolaryngol Head Neck Surg. 2011;10:Doc04.
DOI: 10.3205/cto000077, URN: urn:nbn:de:0183-cto0000772
This article is freely available from
http://www.egms.de/en/journals/cto/2011-10/cto000077.shtml
Published: 2012-04-26
Copyright
©2011 Hummel et al. This is an Open Access article distributed under
the terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You
are free: to Share — to copy, distribute and transmit the work, provided
the original author and source are credited.

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